炎性小体作为抵抗流感病毒免疫的介质。
Inflammasomes as mediators of immunity against influenza virus.
机构信息
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
出版信息
Trends Immunol. 2011 Jan;32(1):34-41. doi: 10.1016/j.it.2010.11.004. Epub 2010 Dec 14.
Abstract
Influenza viruses infect a wide range of avian and mammalian host species including humans. Influenza viruses are a major cause of human respiratory infections and mortality. The innate immune system recognizes influenza viruses through multiple mechanisms. These include endosomal recognition through the Toll-like receptor 7 (TLR7) and cytosolic recognition through the retinoic acid inducible gene I (RIG-I). Recent studies also identified the role of nucleotide binding oligomerization domain (NOD)-like receptors (NLRs) in innate detection of influenza viruses, leading to the activation of the inflammasomes. Here, we review the cellular and molecular mechanisms by which influenza virus infection leads to inflammasome activation, and discuss the consequences of such activation in innate and adaptive immune defense against influenza viruses.
摘要
流感病毒感染包括人类在内的广泛的禽类和哺乳动物宿主物种。流感病毒是导致人类呼吸道感染和死亡的主要原因。先天免疫系统通过多种机制识别流感病毒。这些机制包括通过 Toll 样受体 7（TLR7）的内体识别和通过视黄酸诱导基因 I（RIG-I）的细胞质识别。最近的研究还确定了核苷酸结合寡聚结构域（NOD）样受体（NLRs）在流感病毒先天检测中的作用，导致了炎性小体的激活。在这里，我们综述了流感病毒感染导致炎性小体激活的细胞和分子机制，并讨论了这种激活对流感病毒先天和适应性免疫防御的后果。
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